Acute and chronic graft-versus-host disease (GVHD) are the primary limitations to the increased use of allogeneic bone marrow transplantation. The role of donor T cells, the nature of the effector cells, and the role of suppressor cells in human acute GVHD will be studied. A murine model for acute GVHD due to non-major histocompatibility complex (non-MHC) antigens has been established. The role of donor T cells in the pathogenesis of acute and chronic GVHD in the murine model will be studied. Attempts at recipient manipulation will focus on increasing the percentage of animals with chronic GVHD since a reproduceable animal model does not exist. Patients with chronic GVHD are at increased risk of death due to bacterial sepsis. The basis of the immunodeficiency of chronic GVHD will be studied by evaluating the recipients' immune response to herpes virus antigens. Possible defects in monocyte antigen presentation and the production of lymphocyte mitogenic factors will be evaluated. The mechanism of stable chimerism will be studied in the murine non-MHC model.